It can be difficult to appreciate cardiomegaly in neonates (because of thymus, etc.)

Get a lateral film and use the anterior tracheal line to help determine if cardiomegaly

line parallel to anterior tracheal wall inferiorly to diaphragm – should NOT intersect heart; should NOT be pushed back to “hit” spine above diaphragm

Labs

BNP literature is weak, but can be considered

Initial Management of the Congenital Heart Disease pediatric patient

IV fluids – 10cc/kg

Maintain SpO2 80-85%

Prostaglandin (PGE-1) if considering ductal dependent lesion

Dose is 0.1mcg/kg/hr

Works within 10-15 minutes

Side effects: apnea, hypotension, fever

Historically most pts receiving PGE-1 are intubated however recent data supports watch and wait to see how the patients respond, but have RSI equipment ready

If transferring the patient to another facility after starting PGE-1 you should secure airway to avoid pt becoming apneic en route

Inotropes if shock (did not get into detail on which to use)

Furosemide if pulmonary edema (1mg/kg/dose)

Make sure to check blood sugar

Correct acidosis – early bicarb!

Optimize ionized calcium

Diuretics in Acute Heart Failure: The Dark Side of the Force?

Dr. Peter Pang – Indianapolis EMS

Treatment of heart failure has not changed much over the past 40 years

Only additions are use of inotropes and nesiritide (recombinant BNP)

Patient outcomes have only slightly improved over past 40 years

Current data:

75% = 5 yr mortality for patients admitted for CHF

22% = 30 day rehospitalization rate of patients admitted for CHF

8% = 30 day mortality for patients admitted for CHF

DOSE trial (2011)

No difference in patient outcomes using bolus vs. infusion of Lasix

Doubling (2-2.5x) the dose of patients home dose of Lasix ( continuing patients home dose) was associated with better symptom improvement and increased weight change at 72 hours. However there was no difference in mortality, hospital readmission, or ED visit. And there was increased risk of worsening renal failure with the higher dose.

Best practice appears to be doubling the oral dose of Lasix. You achieve better sx improvement and better urine output. You may get a bump in the Creatine but this doesn’t seem to be worrisome as the patients do well.

Prospective Cohort Study ~1300 pts. Loops that were given within 60 mins of arrival have less in Hosp mortality then delayed therapy. This study is suggestive that early therapy may benefit and is at least safe. Will need more studies to duplicate this finding.

The addition of captopril to combat the RAA system does not have sufficient evidence out at this time to recommend it.

The Evidence For and Against Epinephrine in CPR

Dr. Corey Slovis – Vanderbilt

Epi is a potent alpha and beta agonist

The evidence for use of epinephrine in cardiac arrest is weak and incomplete!

The case for or against epinephrine in CPR is embarrassingly not based on large randomized double-blind studies

Its use stems from a 1968 JAMA study on the use of epi in cardiac arrest of n=15 dogs

There is not good objective evidence, in controlled studies, that epinephrine is more effective than placebo

“High dose” epinephrine, of more than 1 mg per dose, significantly improves ROSC but not survival to discharge

The more you look into the data, the more higher dose of epinephrine looks bad

Also, reduced dose of epinephrine appears to offer no benefits

Early v. late use of epinephrine in cardiac arrest

Use epi as soon as possible (until its effectiveness is proven or disproven)

However, if patient is in VF/pVT, data supports waiting for the second shock prior to giving epi (better outcomes when compared to using after the first shock)

There is a London study coming out soon over >8,000 patients comparing epi vs. no epi for OHCA – should provide some useful information for use of epi in cardiac arrest.

Panel Discussion

RBBB does not prevent our ability to read an EKG like the LBBB does. You just have to look closely for the st elevation in that it can be more subtle. New RBBB in setting of an acute Mi is a bad prognostic sign.

Small group of pts who had pacers were studied with Sgarbossa criteria thus far. Seemed applicable to date. Bigger study by Dr Smith to be out soon that further looks into application of Sgarbossa criteria to paced individuals.

No data on continuous drip of epi verses bolus dose epi in cardiac arrest although some centers are doing this.

Hispanic male in his mid 30s who presented to the ED as John Doe after he was found unresponsive in the field with cardiac arrest. Unknown downtime. As per EMS endorsement from bystanders, the patient allegedly had a witnessed syncopal episode followed by seizure-like activity after which he became unresponsive. No bystander CPR. EMS arrived at the scene and found him pulseless, CPR started. On ALS arrival patient found to be in PEA. CPR, intubated, epi x 2, bicarb then ROSC achieved. Initial rhythm in ED was sinus tach on monitor. After 5 min in ED patient became bradycardic and went into PEA, compressions started, received epi x 1 w ROSC. Pt then went into wide complex tachycardia on monitor – SVT vs Vtach – pt was cardioverted 200J and given Amiodarone 150mg. Post cardioversion, rhythm changed to afib v aflutter. EKG was obtained after 10 min (below).

Patient transferred to the CCU post cath. He was noted to have no brainstem reflexes off sedation. CT Head showed findings c/w anoxic encephalopathy, no bleed. Neuro was consulted who stated patient’s exams and further diagnostic studies were significant for loss of all cortical and brain stem function, consistent with brain death. Patient was pronounced on Day 10 (delay with identifying patient and determining NOK).

Pearls & Takeaways

Is ST-Segment Elevation in Lead aVR Getting Too Much Respect?

Introduction

ECG reading is all about pattern recognition. And this particular pattern of ST-Elevation in aVR with diffuse ST Depression is a very important ECG pattern that you must be able to recognize. But what’s probably more important than being able to recognize the pattern, is understanding what it represents. There appears to be a common misconception that the ST-Elevation in aVR always represents “STEMI”, or acute transmural (full- thickness) ischemia. If this were the case the patient would most likely be dead or at the very least in profound cardiogenic shock. The key to understanding what this pattern represents lies in understanding that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression – and that this diffuse ST-Depression represents global subendocardial ischemia. So the real question that you must answer is: What is causing the global subendocardial ischemia?

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Worrisome Diagnoses:

– Thoracic Aortic Dissection

– Massive Pulmonary Embolism

– Massive Gastro Intestinal Hemorrhage

Non-Worrisome Diagnoses:

– Left Bundle Branch Block (LBBB)

– Left Ventricular Hypertrophy (LVH) with Strain Pattern

– Severe Atrial Tachydysrhythmias (i.e. SVT)

It is critical to realize that more often than not the cause is global myocardial strain from a Non-ACS etiology! (profound sepsis, tachycardia, anemia, hypoxemia, etc). In our patient above it may have been because of the SVT he was in during the code in addition to being in Afib w/ RVR at the time of the ECG. It is also very important to understand that in these Non-ACS settings, you can see this pattern with or without underlying coronary artery disease.

But of course it could be ACS. And if it is, then you are dealing with Left Main, Proximal LAD, or even multi-vessel plaque instability. But keep in mind that even if it is ACS you are still dealing with subendocardial and not transmural ischemia.

Take Home Points

STE in aVR Should be Concerning IF you have a patient with:

Worrisome/Concerning Symptoms (Cardiopulmonary Symptoms) AND…

ST-Segment Depression in Several Other Leads

Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity

Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD Blockage will look “sick” due to global cardiac ischemia. This narrows the number of patients we would consider activating the cath lab for with STE in aVR.

The key to ECG reading is pattern recognition. The pattern of ST-Elevation of at least 1mm in lead aVR + diffuse ST-Depression with a maximal depression vector towards leads II & V5 is a pattern you must know. It represents global subendocardial ischemia.

When you see this pattern you should divide the differential for the diffuse subendocardial ischemia into two main categories: ACS vs Non-ACS. Do not automatically assume that it is ACS. I have seen this mistake made many times as ACS becomes the focus, at the expense of appropriate resuscitation addressing the underlying cause. It is very important to keep in mind that the etiology is far more likely to be Non-ACS than ACS!

The key to determining the etiology is through history, physical exam, clinical picture, laboratory data, Echo, and vigilant monitoring and frequent reassessment. If you have identified and addressed potentially reversible causes of the ischemia, and the ECG pattern persists then you are dealing with ACS until proven otherwise.

Refrain from using dual-antiplatelet therapy in these patients as there is a high likelihood they will require CABG.

Remember that if this ECG pattern does represent ACS, the ST-Elevation in aVR is not the result of direct injury (or transmural ischemia) and that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression. Therefore these ACS cases do not represent a clear “STEMI”. However, while there is not great data to guide the timing of cath for these patients, I would advocate going to the cath lab with a much stronger sense of urgency than for other “NSTEMIs”. The reasoning is that ACS is a very dynamic process and without the advantage of optimal medical therapy (a second platelet inhibitor should be withheld) there is a higher chance of the culprit vessel suddenly occluding and evolving to transmural ischemia. If this happens in the Proximal LAD, Left Main, or in the setting of Multi-vessel involvement the myocardial territory in jeopardy is so large that there is a good chance the patient will arrest and die before any reperfusion can be established! If your patient looks sick or has persistent chest pain, they should be going to the cath lab ASAP.

With diffuse subendocardial ischemia, you may not see any wall motion abnormality. Global function can even be normal, although it may be globally depressed as well. A normal bedside echo does not help in:

HPI: 49-year-old female brought in via ALS presents complaining of Chest pain. As per the Paramedics, the patient was found to be in no acute distress, stating she had exertional chest pain, which had subsided. The pre-hospital ECG was suspicious for ischemia and she was given ASA. Patient states she was walking home from the store when she began to have a pressure like pain on the left side of her chest, which was non-radiating and persisted when she laid down. She admits to feeling similar symptoms over the past few months, but today was the most severe. Upon arrival to Emergency Department, she denied chest pain, SOB, palpitations, abdominal pain, nausea or vomiting. Denied ETOH or illicit drugs use

ED Course: Repeat ECG in ED showed NSR and had completely normalized. Case was discussed with Interventional cardiologist on call. A Code STEMI was activated and patient was taken emergently to the Cath lab. She was given a Heparin bolus as well as Plavix.

ED/Hospital course: The catheterization report revealed 80-90% Distal left main, 30 % mid LAD, and LM stenosis improved partially during catheterization with nitroglycerin. Patient admitted to recently using cocaine. CT surgery was called due to the fact that patient had recent cocaine use and it was believed she might have had Left Main Coronary spasm. On hospital day 2, patient went back for repeat catheterization, which revealed Left main distal 30% and LAD mid 30% stenosis. Patient was transferred to telemetry, and discharged on hospital day 4.

Pearls:

aVR in ACSTypical ECG findings with left main coronary artery (LMCA) occlusion:

(Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity)

ST-Segment Elevation in lead aVR foreshadows a worse prognosis in ACS and often predicts the need for CABG. Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent. ST-segment elevation in aVR can be caused by any of the following 4 mechanisms

Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion (patient will be VERY sick)

Severe multi-vessel coronary artery disease.

Diffuse sub-endocardial ischemia from oxygen supply/demand mismatch.

Patients with complete occlusion of the LMCA (mechanism 2), often present in cardiogenic shock and require immediate revascularization. Patients with acute coronary occlusions typically will have active symptoms and look sick!

There is an estimated 70% mortality without immediate PCI. Medical therapy (including thrombolytic) does not improve mortality. Emergency PCI may decrease mortality to 40%.

What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

HPI: 21-year-old Female presents to the Emergency Department (ED) complaining of palpitations and left arm weakness with perioral numbness, which began just prior to arrival. The patient states the episode lasted 30 minutes before completely resolving on its own. In the ED, she denies any other complaints except for a mild headache. Patient notes she experienced a similar episode of palpitations yesterday afternoon, while resting, which she described as “skipping beats”. On further questioning, the patient admitted to being hospitalized to a NYC hospital 2 weeks ago where she had a Cardiac Echocardiogram done which showed “hypertrophy.” Patient never followed up with cardiologist as instructed. In the past, a doctor in her country prescribed her an unknown antihypertensive medication, which she took for one year but stopped taking it once she moved to NJ. Denies fever, dizziness, chest pain, and shortness of breath, recent travels, calf pain or swelling.

Physical Exam:

BP 109/72 HR 82 RR 18 SpO2 100% on RA Temp 97.0F

General: Well appearing female, in non-acute distress

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Cardiac: +S1/S2, no MRG, regular rhythm

Abdomen: soft NT ND

Neuro exam: AAO X 3, No focal deficits

Extremities: no edema, no tenderness or swelling, 5/5 strength in all extremities. Sensory intact

Skin: pink and warm, No diaphoresis, no rashes, lacerations, or abrasions

Pertinent Labs: Troponin 0.308

Pertinent Imaging and other tests:

Chest X-Ray: Cardiomegaly with a boot shaped heart, which may indicated right heart failure.

CT Head: Normal

ECG: Normal Sinus Rhythm, Bi-atrial enlargement, RBBB, LVH

Working Diagnosis: Hypertrophic Cardiomyopathy (HCOM)

ED/Hospital course: Patient was given 324 mg of ASA and admitted to Telemetry with a diagnosis of Hypertrophic Cardiomyopathy. While still in the ED waiting for a bed on Telemetry the patient had multiple runs of non-sustained V-Tach and Cardiology was consulted. The patient was started on ASA and Metoprolol PO. A 2D ECHO was done which was consistent with HCOM. Patient remained stable on Telemetry for 3 days prior to discharge. The patient’s Troponin was trended daily, 0.308 in the ED, 0.288 on day 1 of admission, and 0.314 on day 2 of admission. Patient was told to follow up with Cardiology Clinic for possible AICD placement planning.

Pearls:

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac disorders (affecting ~ 1 in 500 people) and is the number one cause of sudden cardiac death in young athletes. Annual mortality is estimated at 1-2 %.

Pathology and Pathophysiology:

Dynamic Obstruction of the Left Ventricular Outflow Obstruction (LVOT)

Primarily Autosomal Dominant Inheritance

Left Ventricular diastolic dysfunction resulting from impaired relaxation and filling of the stiff and hypertrophied left ventricle (often associated with increased filling pressure)

Check out this excellent review on managing patients with LVADs from this month’s ACEP Now publication which was written by our own Dr. Yenisleidy Paez Perez, DO PGY-3 and one of our newly graduated residents, Dr. Terrance McGovern, DO. The article is entitled ‘How to Manage Emergency Department Patients with Left Ventricular Assist Devices.” Click the link below to be forwarded to the article.

Pearl’s from Wed conference August 2nd 2017:

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium, and BiPAP.
-Intubation last resort for asthma. Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD. Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)

Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time. To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost. Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.

Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU. If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.

Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
-Can use a double lumen ET tube with a endobronchial cuff
-The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Take home points from 2012 Retrospective Cohort Study:
-With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
-So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

HPI: 32 yo female with PMH of Romano Ward Syndrome s/p AICD, previous cardiac arrest, Atrial Fibrillation s/p Ablation, renal artery thrombosis on Coumadin and deafness presents to the Emegency Department (ED) via ALS after being found unresponsive at home and with ventricular tachycardia. Paramedics state they were called to the patient’s home for an “unconscious” person. They arrived to find the patient lethargic but arousable, cool, pale, and diaphoretic with BP 90/50. The patient soon became unresponsive and was in Ventricular tachycardia on the monitor. Patient underwent synchronized cardioversion with 150 Joules and converted to sinus tachycardia. Patient also received 150 mg Amiodarone bolus and 250 mL of Normal Saline IVF. Patient’s sister arrived to ED approximately 10 minutes after patient’s arrival and states that patient had multiple episodes of becoming unconscious at home earlier today. Denied recent illness, fever/chills, vomiting, diarrhea

ED Course: Approximately 5 minutes after arrival to the ED during the initial exam, patient became unresponsive and was noted to be in Ventricular Fibrillation on the monitor. CPR/ACLS was started and patient was intubated immediately. Her defibrillator appeared to be delivering shocks however there was no conversion of the rhythm. ACLS was performed for 30 minutes and pulses were regained multiple times. Patient was in V-fib, then PEA, then V-tach arrest. 100mg Lidocaine and 2 grams Magnesium were also given. Defibrillation with external pads ultimately led to Return of Spontaneous circulation. Bloody, frothy sputum was also noted from the ETT post-arrest. A right IJ central line was placed

ED/Hospital course: Post-ROSC EKG did not show STEMI. Post-ROSC Chest XR demonstrated diffused pulmonary edema. Patient was hypoxic with SpO2 in the 80s on 100% FiO2. Decreased tidal volume and increased PEEP improved oxygenation. Bedside cardiac Ultrasound showed global hypokinesis and no pericardial effusion. CT Head w/o contrast was normal. Amiodarone drip was started. Hypothermia protocol was initiated. The patient was admitted to the CCU. She did not code again while in the ED. Her AICD was interrogated and it showed she had been in sustained Vtach to which her AICD gave multiple shocks without capture. She was in the hospital for 11 days where she initially was improving and was therefore extubated after 7 days. Unfortunately she again went into Vtach arrest multiple times and then PEA arrest and was pronounced dead.

Pearls:

Congenital Long QT Syndrome (LQTS)

The major variant of congenital prolonged QT syndrome (there are 6 total). Affects estimated 1/2500 to 1/7000 people worldwide

Romano-Ward is the more common, autosomal dominant (AD) form with purely cardiac phenotype.

The Jervell and Lange-Nielsen syndrome refers to the autosomal recessive (AR) phenotype of congenital LQTS that is associated with profound sensorineural hearing loss and a high risk for sudden death. MORE MALIGNANT CLINICAL COURSE. Our patient likely had this variation since she also had deafness.

HPI: 47 year old female with PMHX of HTN and ETOH abuse presents with abdominal pain. Patient states that beginning two days ago she was woken up from her sleep with sudden onset non-bloody vomiting as well as epigastric pain which radiates to the back and is sharp in nature. She admits to over 15 episodes of vomiting. She is also having cramping of her feet bilaterally. She admits to daily ETOH use, and states her last intake was two days ago, denies illicit drug use. Denies taking any medication prior to arrival. Denies fever, chills, chest pain, SOB or dysuria. Denies recent travel or sick contacts. PMHX/PSHX: none Meds: none Allergies: none

ED/Hospital course: Upon arrival to ED patient had Epigastric pain with vomiting, Patient started on IVF and received Pepcid and Zofran. EKG at this time showed QT prolongation and patient found to have magnesium of 1.3. While waiting for magnesium, she started to have short runs of polymorphic ventricular tachycardia and during these times she complained of chest tightness. After 2 grams of magnesium patients repeat EKG showed normal QT and runs of ventricular tachycardia stopped. She received another 2mg of Magnesium and 40 mEq of Potassium Chloride. Patient was then admitted to Telemetry floor. Patient observed for 24hours and discharged to home with follow up with a cardiologist and Norvasc 5 mg 1tab PO daily, Losartan 100 mg 1tab PO daily, Ranitidine 150mg 1tab PO BI.

Pearls:

An abnormally prolonged QTc, especially >500 is associated with an increased risk of ventricular arrhythmias, Torsade’s de Pointes

Prolonged QT with prolonged ST-segment is due to: HypoCa, Hypothermia.

If EKG reveals long QT start by reviewing drug history and checking electrolytes. Stop any offending agents. Suppress early after depolarization with IV magnesium sulfate and keep potassium >4.5meq/L.

If non responsive to magnesium, may consider cardiac pacing and rarely isoproterenol infusion. Acceleration of the heart rate may produce suppression of arrhythmias, with a reduction in the QT interval.

Below is a review of the key points of each lecture from the 2017 University of Maryland Emergency Cardiology Symposium which was hosted by Amal Mattu, MD in Baltimore, MD. This year’s topic was Cardiac Arrest.

Journal of Resuscitation: 120-140 compressions per minute (compared to ACLS taught 100-120) showed improved ROSC at this rate in the year 2017. Single center. Roughly 200 something patients.

5-6 cm depth of compressions with appropriate recoil of chest wall.

Avoid leaning on the chest.

Chest compression fraction (percentage of time in which chest compressions are done by rescuers during cardiac arrest) should be greater than 60%; goal of 80%.

Hemodynamic-Directed CPR

Using femoral arterial line, aim for DBP >25-35 mmHg. This is also helpful for determining PEA vs pseudo-PEA.

Using end tidal CO2, aim for >20 mmHg.

Hold epinephrine if these parameters are met.

Aim for a coronary perfusion pressure (CPP = aortic diastolic pressure minus the left ventricular end-diastolic pressure) of >20 mmHg to attain ROSC. Need arterial and central line to obtain the CPP which may be difficult during a resuscitation. Instead, we can guide our resuscitations with the use of early arterial line placement and/or end tidal CO2.

Consider video laryngoscopy as first attempt in CPR because DL increases “no flow” time seen bc of holding compressions to optimize view. Success rate is similar.

Code Medications: Epinephrine: ? evidence of efficacy. There exists no definitive evidence of epi’s benefit to long term survival to date.

NEJM 2016: Amiodarone vs Lidocaine vs Placebo in out of hospital cardiac arrest shockable rhythms: NO DIFFERENCE. However, there was a non-statistically significant trend towards benefit to hospital discharge in those getting amio or lido vs placebo.

ECHO Evaluation in Cardiac Arrest

Sarah A. Stahmer, MD; UNC

US can interrupt cardiac compressions. Need to use a focused approach to limit delay during CPR

A twitch in the heart muscle is not cardiac stand still. Must be no cardiac muscle movement for standstill. However, valvular motion with cardiac stand still is considered cardiac death.

Sonographic asystole has a poor prognosis, but not no prognosis. Small chance of survival exists. If patient young, continue resuscitative efforts. Older/Nursing home patients it may be reasonable to call the code.

Must consider all patient variables with continuation of resuscitative efforts.

Cool to 36 if mild sx moving around etc. Cool to 33 if in deep coma /sicker subset (Personal preference)

ECMO is reimbursed very well as long as your pt is insured

Fingers to palpate a pulse are not very good. Ultrasound, arterial line, and end tidal may be better resources. One study done in prehospital setting with ultrasound in the field shows those with no pulse but ultrasound showing cardiac motion did better with Meds (pressors) verses starting compressions. These patients have “pseudo pea” bc they actually have a pulse you just can’t feel it.

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Disclaimer: Information contained on this website is the opinion of the authors and does not represent the opinion of St. Joseph's Regional Medical Center or St. Joseph's Regional Medical Center Emergency Medicine Residency Program.